Glycation – Sugar Coated Cellular Dysfunction

Over the next several weeks, I’ll be posting excerpts from the book and blogging frequently about the main concept in the book – which is the idea of harnessing your body’s internal cellular biochemistry to achieve true balance in body, mind, and spirit – and in doing so, help you to become your “Best Future You” in terms of how you look, how you feel, and how you perform on every level.

Chapter 5 – Pillars of Health

Glycation – Sugar Coated Cellular Dysfunction

Glycation is a process by which a sugar molecule (typically glucose or fructose) becomes bonded to a protein or lipid (fat). Most often, glycation occurs in the body when glucose or fructose in the blood remains too high for too long and becomes bonded to cell-surface proteins. A glycated protein—referred to as an “AGE” (advanced glycation end-product)—can be highly reactive and set off a chain reaction of oxidative and inflammatory damage in whatever tissues they occur. AGEs also tend to be “cleared” from the body very slowly, so once they’re formed, they have the potential to stimulate these damaging chain reactions for prolonged periods of time.

Some of the main dietary offenders that lead to AGE accumulation and upset biochemical balance are high-sugar foods (such as soda, ice cream, donuts, cookies, or sweetened breakfast cereals) and other foods that quickly convert to sugar or glucose in the bloodstream (including highly processed grains, such as white bread, rolls, or instant rice). Sugar can be toxic to many tissues by permanently attaching to proteins through the glycation process. Wherever sugar attaches, it triggers cellular microdamage that creates inflammation. The inflammation, in turn, accelerates protein breakdown, thus resulting in damage to surrounding tissues. To make matters worse, glycation also leads to cross-linking of proteins, changing healthy tissues from soft, supple, and flexible to stiff, brittle, and painful. These stiffened sugar-protein bonds form in every type of tissue, including joint cartilage, muscle tendons, brain neurons, blood vessels, skin, and even immune-system cells, which is why scientists are finding links between glycation and chronic diseases of “aging,” such as cardiovascular disease, Alzheimer’s disease, and arthritis.

There are many reasons to keep a tight control of glucose levels. Glucose, which you may often hear called “blood sugar,” is the preferred source of energy for the brain, and glucose helps you fully metabolize calories from fat. Blood sugar levels that drop too low may stimulate hunger and cravings, while glucose levels that rise too high will slow your ability to burn fat.

A key intermediary in the interrelationships between blood glucose (glycation), free radicals (oxidation), cytokines (inflammation), and stress hormones (allostation) is the hormone insulin. Most people associate insulin problems with diabetes because of its primary role in regulating blood-sugar levels, but insulin has many additional functions in the body. Not only does insulin regulate blood-sugar levels within an extremely narrow range, but it is also responsible for getting fat stored in the fat cells (adipose tissue), getting sugar stored in the liver and muscle cells (as glycogen), and getting amino acids directed toward protein synthesis (to build muscle). Due to these varied actions, insulin is sometimes thought of as a “storage hormone,” because it helps the body put all these sources of energy away in their respective “storage depots” for use later.

The abnormal insulin metabolism described above—known as insulin resistance—leads to a reduction in the body’s cellular response to insulin. That reaction, in turn, interferes with regulation of blood sugar, increases appetite, and blocks the body’s ability to burn fat due primarily to direct “blocking” of insulin function by cortisol as well as indirect interference with insulin activity by oxidative free radicals and inflammatory cytokines. When insulin resistance is combined with a poor diet (high in fat and/or refined carbohydrates), the result is the metabolic condition known as Syndrome X, a disorder that can have an impact on virtually every disease process in the body.

We know that inflammation in any tissue can be caused by excessive exposure to free radicals and lead to accelerated “aging” and generalized tissue breakdown. AGEs demonstrate a “direct” problem with cell-to-cell signaling that is compromised by sugar-coated proteins. “Indirect” damage is also caused by an AGE-stimulated increase in oxidation and inflammation. Stress hormones, which we’ll discuss in the next section, stimulate the creation of AGEs through an increase in blood-sugar levels.

People with diabetes are obviously at high risk for developing AGEs in a wide range of tissues because of their problems regulating blood-sugar levels. The extreme development of AGEs in diabetics is a key reason for their high rates of oxidative and inflammatory diseases, including nephropathy (kidney damage) and circulatory problems (due to blood-vessel damage).

There are numerous ways to stabilize glucose and reduce your development of AGEs—some of which might seem quite obvious, as you’ll see in the short list below, but are also quite effective.

The next section, about “allostation” and stress hormones such as cortisol, describes how cortisol exposure stimulates a rapid increase in blood-glucose levels via several mechanisms, including stimulating the release of glucose stored in the liver, interfering with insulin’s action to stimulate cells to absorb glucose from the blood, and stimulating overall appetite with specific cravings for sweets. Adding to the connection between cortisol and insulin resistance are an interesting series of studies showing that inadequate sleep causes insulin resistance. This is particularly important because of the well-known link between sleep deprivation as a unique type of cellular stress and elevated cortisol levels. Sleep researchers from the University of Chicago and several other universities have shown that inadequate sleep leads to a cascade of biochemical events, starting with increased cortisol levels, which induces insulin resistance, leading to higher blood-sugar (glucose) levels, causing increased measures of oxidative and inflammatory damage, stimulating appetite, and eventually leading to abdominal fat (belly fat) gain. The research team compared “normal” sleepers (averaging eight hours of sleep per night) to “short” sleepers (averaging six hours or less of sleep per night). They found that the “short” sleepers secreted 50 percent more cortisol and insulin and were 40 percent less sensitive to the effects of insulin than the “normal” sleepers. Missing a couple hours of sleep can basically put you into a pre-diabetic state with all the associated cellular stress and eventual health problems.

Thanks for reading – please tune in for the next installment about “Allostation” (chronic stress).